ArticleeLife2022
SARS-CoV-2 Nsp14 mediates the effects of viral infection on the host cell transcriptome.
Article in eLife, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 66 citations in OpenAlex.
- Coronavirus NSP14 drives internal m7G modification to rewire host splicing and promote viral replication.Nucleic acids research · 2026Article
- Dual antiviral and anti-inflammatory effects of BAY 11-7082 in SARS-CoV-2 infection via inhibition of the canonical NF-κB signaling pathway.Scientific reports · 2026Article
- SARS-CoV-2 nsp14 induces the mCommunications biology · 2025Article
- SARS-CoV-2 NSP14 inhibitor exhibits potent antiviral activity and reverses NSP14-driven host modulation.Nature communications · 2025Article
- Viral Modulation of Host Splicing.Annual review of virology · 2025Review
- Article
- Decoding the transcriptome from bulk RNA of infection-naïve versus imprinted patients with SARS-CoV-2 Omicron B.1.1.529.Microbiology spectrum · 2025Article
- Viral Reprogramming of Nucleotide Synthesis and Its Impact on Viral Infection.Journal of medical virology · 2025Review
- A single mutation may contribute to accelerated evolution of SARS-CoV-2 toward Omicron.Nature communications · 2025Article
- Impact of SARS-CoV-2 Wuhan and Omicron Variant Proteins on Type I Interferon Response.Viruses · 2025Article
- A High-Throughput Screening Pipeline to Identify Methyltransferase and Exonuclease Inhibitors of SARS-CoV-2 NSP14.Biochemistry · 2025Article
- Circular RNAs in the pathogenesis of SARS-CoV-2: potential diagnostic biomarkers and therapeutic targets.Functional & integrative genomics · 2025Review
- Linear ubiquitination mediates coronavirus NSP14-induced NF-κB activation.Cell communication and signaling : CCS · 2024Article
- Nanobody against SARS-CoV-2 non-structural protein Nsp9 inhibits viral replication in human airway epithelia.Molecular therapy. Nucleic acids · 2024Article
- Comparative Atlas of SARS-CoV-2 Substitution Mutations: A Focus on Iranian Strains Amidst Global Trends.Viruses · 2024Article
- Comparative analysis of dynamic transcriptomes reveals specific COVID-19 features and pathogenesis of immunocompromised populations.mSystems · 2024Article
- Progressive Evolutionary Dynamics of Gene-Specific ω Led to the Emergence of Novel SARS-CoV-2 Strains Having Super-Infectivity and Virulence with Vaccine Neutralization.International journal of molecular sciences · 2024Article
- SARS-CoV-2 Selectively Induces the Expression of Unproductive Splicing Isoforms of Interferon, Class I MHC, and Splicing Machinery Genes.International journal of molecular sciences · 2024Article
- Evolution and Impact of Nucleic Acid Amplification Test (NAAT) for Diagnosis of Coronavirus Disease.Analytical chemistry · 2024Review
- 1-L Transcription of SARS-CoV-2 Spike Protein S1 Subunit.International journal of molecular sciences · 2024Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Viral infection involves complex set of events orchestrated by multiple viral proteins. To identify functions of SARS-CoV-2 proteins, we performed transcriptomic analyses of cells expressing individual viral proteins. Expression of Nsp14, a protein involved in viral RNA replication, provoked a dramatic remodeling of the transcriptome that strongly resembled that observed following SARS-CoV-2 infection. Moreover, Nsp14 expression altered the splicing of more than 1000 genes and resulted in a dramatic increase in the number of circRNAs, which are linked to innate immunity. These effects were independent of the Nsp14 exonuclease activity and required the N7-guanine-methyltransferase domain of the protein. Activation of the NFkB pathway and increased expression of
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.